Hi Emmy: The "Type 2s" who are antibody positive (about 10% of "Type 2s") are actually misdiagnosed Type 1s. Type 2 is not autoimmune. According to the Expert Committee on the Diagnosis and Classification of Diabetes Mellitus:“Type 1 diabetes results from a cellular-mediated autoimmune destruction of the beta-cells of the pancreas. In Type 1 diabetes, the rate of beta-cell destruction is quite variable, being rapid in some individuals (mainly infants and children) and slow in others (mainly adults)” and "Although the specific etiologies of Type 2 diabetes are not known, autoimmune destruction of beta-cells does not occur."
The big mystery in T2 has always been why does insulin resistance start. This study, which confirms the results of an earlier study, sheds light on that question and opens up a new avenue for further research.
I wonder how long the popular press will take to pick up on this and get off their you gave yourself T2 schtick?
I wonder as well if instead of T2, it might be more appropriate to look at it as different diseases of different, albeit related systems? Biology is so complicated it seems as if you had a couple of "equations" running in a different way it could create the sort of layered challenges people report w/ T2? Maybe it ought to be T5 or T6 instead of just "2"?
My understanding is that there are around 14 different genes involved in T2. Just the fact that some classified as T2 are thin points to the correctness of your view.
Hi Emmy: You said, “studies have shown that T2's can have the same antibodies that type 1's do” but the studies you provided links to don’t show that at all, quite the opposite. The studies you provided links to are interesting, but they do not discuss diabetes caused by immune-mediated destruction of the beta cells of the pancreas nor the autoantibodies (GAD, ICA, IA-2, Zn8) indicative of Type 1 diabetes.
The ‘10% of “Type 2s” who are antibody positive’ refers to results of studies that have been done all over the world over the past 30+ years that show that about 10% of people given the diagnosis of Type 2 diabetes are antibody positive (GAD, ICA, IA-2, and/or Zn8), have been misdiagnosed, and in fact have Type 1 diabetes. The UKPDS is an example of a study where 10% of “Type 2s” were antibody positive and had initially been misdiagnosed.
For the young, thin, athletic women who are portrayed in this Women’s Health article, it is highly unlikely that they have Type 2 diabetes. Far more probable is that they have Type 1 diabetes or monogenic diabetes.
Assuming some or all of those "T2's were not misdiagnosed T1's. Which is a big assumption as so many are.
I'm definitely not a scientifically oriented mind, but what do multiple genes have to do with antibodies?
From a strictly lay perspective, I have no doubt that the etiology of Type 2 is far more complex than the horrible media picture of "you ate too much junk, gained weight and gave yourself diabetes." Nevertheless, in the act of rejecting this awful stereotype that is also a great oversimplification, I think it might be premature to say "oh, it's an autoimmune disease like type 1."
My own experience illustrates I think some people's Diabetes which exists in a "bordertown" and then something motivates the D to cross over to one or the other side of the border. They then live in a completely new country. I fought 10-40 pounds of overweight all my life as did my father and his mother who I resemble. That grandmother did, I believe have type 2 and at least when I knew her in old age was quite overweight. I also struggled with high bp and cholesterol, both markers of type 2. But I also have, as I've described on here, a strangely powerful immune system that has fought off disease all my life. In 1994 I was diagnosed with Graves Disease and then in 2007 with Type 2 Diabetes which I recognized Was Type 1 in 2009 when the oral drugs stopped working. At the time of diagnosis I lost 40 pounds. So am I a Type 1 that could have "gone to the other side of the border and become a Type 2?"
I think there will always be the outliers that don't fit any preconceived mold, and to some extent that indicates knowledge we don't yet have. When I went through my head bending effort to discover my true diagnosis as LADA/Type 1, I told my conclusion to a friend who is an RN. She said, ahhh..that explains some things. We've always seen a number of people with Diabetes that didn't seem to fit into recognizable categories.
There is no misinterpretation. I am saying that Type 2 diabetes does not involve immune-mediated destruction of the beta cells of the pancreas. Some Type 2 may have an autoimmune component, as these studies suggest, but T2 does not involve immune-mediated destruction of the beta cells.
I knew that after I posted my thoughts using metaphors and subjective experience, Melitta would appear and give it the scientific base I knew was there all along! (Just like you do when I say "full panel of antibody testing" and then you list the unpronouncable names that entails.) ::::waves:::: Hi, my scientific friend!
Hi Zoe: Yes, still just trying to prevent misdiagnosis or get people more quickly to the correct diagnosis! You and I know about that. I hope someone suggests to those poor women in the Women's Health article that they go to a competent endo....
It never ceases to amaze me how doctors (and endos!) can get away with presenting such inaccurate, incomplete and outdated information to their patients when so much information is available on the internet and in the DOC. Oh, that's right doctors look down on internet info as being unprofessional and not credible!
In trying to start a Type 1 group here in the northstate I'm considering sending a flyer to the medical group in Redding that misdiagnosed me. Since I left the country shortly thereafter they would have no way of knowing what happened. I'd love to see their faces when they read, "Zoe Heyman, Type 1 Diabetic???
I think if doctors would err on the side of type 1 instead of type 2 it could solve this problem. A type 2 getting insulin is not going to kill him or her but lack of it can kill a type 1.
The antibodies test can be unclear but it should be done to at least rule it out.
I think if the 2 diseases type 1( auto immune ) and type 2 ( insulin resistant) were called different things entirely, it could help .
I was misdiagnosed as well, and had we not pressed an Endocronologist to perform antibody testing in the early stages, I would be wondering why my sugars are continuing to climb even as I have cut carb intake to 125 a day and am exercising 10-12 hours a week vigorously. I now just need to find an Endo that understands Type 1, I see a new one next Friday, wish me luck.
Hi Parrformance: Best of luck, I hope the new endo is good! It is so important to get appropriate treatment. And good for you for being your own best advocate.
Thank you Miss Melitta, you were the catalyst to search out another endo/second opinion:)
@lisa: That doesn't work for me, and doesn't work for many others I know. I am overweight but GAD Positive with no c-peptide (33 years in). My daughter at 22, is thin, with an awful 1st phase insulin response (high BGs), which is the start of something. We are just waiting for antibody tests to come back for her. There are indeed thin T2s, who are not antibody positive and do not have MODY. There is a possibility she has PCOS with three burst ovarian cysts so far, but they were all singles and scans at the time don't put her in the PCOS class, according to her doctors, because they are looking for multiple cysts.
We are assuming here that we (researchers etc) know all there is to know about diabetes. I suggest we don't know and that we will find in years to come, more causes for insulin resistance in thin people, and more variants of all kinds of diabetes.
Nevertheless, for the percentage of diagnosed T2s who are actually slow-onset T1, it's a disservice to them that more doctors are not prepared to do any testing (for whatever idiotic reason) because it's thought that early insulin can prolong the health of existing beta cells. It also stops these people from being called non-compliant (as I was for many years), and hanging around with high BGs that often are not being addressed.
The tests are easily done and in my opinion, should be routine. I, like others, spent years fighting to be tested when doctors were saying, "impossible" because I'm in the overweight category of BMI. It shouldn't have had to be that hard! Meanwhile, I spent more than 10 years with huge spikes and some resulting damage and it slid me into diabetes burnout because I just wasn't prepared to go marathon running every time I ate something, to get by BGs down. It's really a tragedy in every sense of the word, because it all could have been avoided.
I think the miscommunication here is around the historic use of the term "autoimmune diabetes" as short-hand for "autoimmune destruction of the beta cells in the pancreas resulting in T1 diabetes".
What the NEW research is showing it that there are OTHER kinds of autoimmune processes creating insulin resistance, which can be found in both T1's and in T2's.
To clarify: you don't have to be T2 to have autoimmune-related insulin resistance, but only T1's have autoimmune-related destruction of the beta cells.
I will not tread into the murky and shark-infested waters of "double diabetes" here, but the bottom line is that you can no more give yourself T2 by eating too many M&M's than you can give yourself T1 by eating too many M%M's. All types of diabetes have a genetic component that MUST be present for diabetes to develop.
Agreed, especially as "insulin resistant" is probably also "autoimmune" -- just a different kind of autoimmune that results in insulin resistance rather than the direct destruction of beta cells.
Just to make this even more maddening, T2 also results in the destruction of beta cells over time, just not as rapidly nor via the same process that causes T1:
"In type II diabetes, an increasing demand for insulin places a substantial stress on the protein secretion system of the beta cells of the islets of Langerhans, which results in cellular dysfunction and, eventually, beta cell death. As the population of beta cells continues to diminish, the stress on the remaining cells increases as they struggle to produce the insulin necessary to mount a proper host homeostatic response. This feedback loop is thought to be responsible for the progressive nature of type II diabetes (1).
Cross-β-sheet amyloid deposits are generally observed in the islets of Langerhans of type II diabetic subjects (2) and their presence correlates with the loss of beta cells (3). Whether amyloidogenesis causes, exacerbates, or results from beta cell dysfunction in humans are key unanswered questions being intensely investigated (2–5). The primary component of the amyloid deposits is amylin or islet amyloid polypeptide (IAPP), a peptide that is co-secreted with insulin by islet beta cells (3). Human amylin is a highly amyloidogenic peptide based on in vitro experiments, and amylin amyloidogenicity in organismal diabetes models correlates with beta cell death, although to date, a direct cause and effect relationship has been difficult to establish (2, 6–8)."